Radiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Published online before print June 23, 2004, 10.1148/radiol.2322030334
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2322030334v1
232/2/606    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Muthupillai, R.
Right arrow Articles by Dixon, W. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muthupillai, R.
Right arrow Articles by Dixon, W. T.
(Radiology 2004;232:606-610.)
© RSNA, 2004

Technical Developments

Acute Myocardial Infarction: Tissue Characterization with T1{rho}-weighted MR Imaging—Initial Experience1

Raja Muthupillai, PhD, Scott D. Flamm, MD, James M. Wilson, MD, Roderic I. Pettigrew, MD, PhD and W. Thomas Dixon, PhD2

1 From Philips Medical Systems, Cleveland, Ohio (R.M.); Departments of Radiology (R.M., S.D.F.) and Cardiology (S.D.F., J.M.W.), St Luke’s Episcopal Hospital and Baylor College of Medicine, 6720 Bertner Ave, MC 2–256, Houston, TX 77030; and Department of Radiology, Emory University Hospital, Atlanta, Ga (R.I.P., W.T.D.). Received February 27, 2003; revision requested May 20; final revision received November 25; accepted December 17. W.T.D. and R.I.P. supported by grant no. RO1 HL58417. Address correspondence to R.M. (e-mail: raja.muthupillai@philips.com).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 
Acute myocardial injury was evaluated in 21 patients by using a contrast material–enhanced T1{rho}-weighted cine turbo field-echo magnetic resonance (MR) imaging sequence and a delayed-enhancement sequence. In 12 of 21 patients, conventional T1-weighted contrast-enhanced cine turbo field-echo MR images were also collected for direct comparison with T1{rho}-weighted images. Delayed-enhancement technique distinctly characterized irreversible injury (percentage enhancement, 588% ± 344). With T1{rho} weighting, percentage enhancement of irreversibly injured myocardium was 68% ± 41, compared with 23% ± 24 without T1{rho} weighting (P < .006). The addition of T1{rho} weighting to contrast-enhanced cine turbo field-echo MR sequences may offer a new contrast enhancement mechanism for characterization of acutely infarcted myocardium.

© RSNA, 2004

Index terms: Magnetic resonance (MR), cine study, 511.12142, 511.12143 • Magnetic resonance (MR), tissue characterization, 511.12146 • Myocardium, infarction, 511.76, 511.771 • Myocardium, MR, 511.12142, 511.12143, 511.12146


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
Materials and Methods
Results
 Discussion
 REFERENCES
 
Several techniques have been proposed to assess the nature and extent of myocardial injury after acute myocardial infarction by using magnetic resonance (MR) imaging (1–4). It has been shown in animal and human studies that it is possible to identify irreversibly injured myocardium by using a delayed-enhancement technique (5,6). Several studies (5–7) have showed that in regions that are irreversibly injured, the distribution volume for the paramagnetic contrast agent gadopentetate dimeglumine is increased, and the wash-in and washout rates of contrast agent are altered. As a result, contrast agent accumulates in the necrotic tissue 15–20 minutes after administration, resulting in T1 shortening in those regions (8). This T1 shortening is exploited in the delayed-enhancement technique to reveal areas of irreversible injury by using inversion-recovery preparation to highlight T1 differences (9,10).

Several other MR imaging methods have been proposed to identify irreversibly injured myocardium on the basis of the structural, hemodynamic, or metabolic changes that accompany such injury—for example, imaging changes in apparent diffusion coefficient of water associated with the onset of irreversible injury (11) or changes in systolic wall stress that reflect ventricular remodeling after acute myocardial infarction occurs (12).

Studies have shown that T1 relaxation in the rotating frame of reference (T1{rho}) is a sensitive marker for probing macromolecular-water interaction (13,14) and provides valuable information in characterization of cartilage (15), tumors (16,17), and acutely infarcted cerebral tissue (18). An intact human myocyte is primarily composed of two types of macromolecules: structural proteins and contractile proteins, such as collagen, actin and myosin (approximately 50% cell volume), and mitochondria (approximately 33% of cell volume) (19). Ischemic infarction results in cell death by means of either compromised integrity of the sarcolemmal membrane (necrosis) or intracellular degeneration and nuclear disintegration (apoptosis). Since both processes alter the macromolecular water interactions in the infarcted myocardium (compared with normal myocardium), we hypothesized that T1{rho} of infarcted myocardium could be different from that of normal myocardium.

In this work, we sought to test the hypothesis that T1{rho} spin preparation can be used in contrast material–enhanced cine MR imaging to differentiate normal from injured myocardium following acute myocardial infarction.


   Materials and Methods
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 
Patient Population
The study was approved by the institutional review board of St Luke’s Episcopal Hospital, and all patients gave informed consent prior to imaging. Twenty-one patients (16 men with a mean age of 57 years ± 12 and an age range of 32–87 years; five women with a mean age of 67 years ± 14 and an age range of 51–82 years; men and women combined [n = 21], mean age of 59 years ± 13 and age range of 32–87 years) who were referred for MR imaging after reperfused acute myocardial infarction were imaged 63 hours ± 40 after the acute event.

All patients satisfied the World Health Organization criteria for acute myocardial infarction (20). All patients had abnormal serum cardiac enzyme levels, as evidenced by creatine kinase of cardiac origin, or CK-MG, levels more than three times higher than the upper limits of normal values, and all but one patient had electrocardiographic evidence of acute myocardial infarction. These were not consecutive patients, since patient recruitment depended on the availability of the MR imaging system and research nurse staff during normal working hours.

MR Image Acquisition
All studies were performed with a 1.5-T Gyroscan NT imager (Philips, Best, the Netherlands) with R.6.2.1 software. Data were collected by using a five-element surface cardiac coil for improved signal reception. Images were acquired after a single intravenous injection of 0.2 mmol per kilogram of body weight of gadopentetate dimeglumine.

All patients were imaged by using delayed enhancement, as well as T1{rho}-weighted cine turbo field-echo MR acquisitions in a series of breath holds. The total acquisition time for MR imaging was restricted to approximately 1 hour for each patient. In amenable patients who tolerated prolonged imaging (n = 12), conventional cine turbo field-echo MR images were acquired in addition to T1{rho}-weighted images for comparison. In these patients, the images with and those without T1{rho} weighting were acquired within 10 minutes of each other, following administration of contrast material. Descriptions of the specific acquisition parameters for each technique follow.

T1{rho}-weighted acquisition.—Dixon et al (21) described a method for achieving T1{rho} weighting in a conventional cine turbo field-echo MR sequence by using a composite radiofrequency pulse to improve contrast of blood to normal myocardium. A more detailed description of the pulse sequence is described elsewhere (21), but specific acquisition parameters used in the present study are provided.

A conventional T1-weighted electrocardiographically triggered T1-weighted cine turbo field-echo sequence was modified to include a composite radiofrequency pulse before each shot to provide T1{rho} weighting, as shown in Figure 1. The five-element composite radiofrequency pulse used was 90y-135x-360x-135x-90-y, with element durations of 0.84, 1.26, 8.12, 1.26, and 0.84 msec, respectively. Other acquisition parameters were repetition time msec/echo time msec, 5.0–5.2/2.1–2.3; flip angle, 25°; field of view, 320–380 mm; section thickness, 8–10 mm; matrix, 128 x 256; acquisition time, 16–18 heartbeats per section; and 16–18 shots used to collect all 128 images per cardiac phase in a breath hold. The temporal resolution of each acquisition varied from 46 to 72 msec, depending on the heart rate. Standard cardiac views included short axis, two-chamber long axis, and four-chamber long axis.



View larger version (14K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1. Timing diagram of the T1{rho}-weighted cine turbo field-echo MR sequence. Each turbo field-echo shot consisted of a composite radiofrequency pulse for spin lock and a segmented k-space readout consisting of n observation pulses, each with flip angle {alpha}. The conventional turbo field-echo sequence did not include the T1{rho}-weighted prepulse before the turbo field-echo readout.

 
T1-weighted acquisition.—In 12 of 21 patients, conventional T1-weighted cine turbo field-echo MR images were collected without the composite radiofrequency pulse used for T1{rho} weighting for comparison. Other acquisition parameters were 4.0–6.0/1.5–2.3 and flip angle of 25°; field of view, matrix size, and acquisition orientation were identical to those in the T1{rho}-weighted acquisition. The temporal resolution of the acquisition ranged from 34 to 60 msec, depending on the heart rate.

Delayed enhancement acquisition.—In 21 of 21 patients, a turbo field-echo MR sequence with an inversion prepulse was used to collect delayed-enhancement MR images 15–20 minutes after administration of contrast material. The electrocardiographically triggered sequence consisted of an inversion prepulse, user-defined inversion delay, and a short burst of gradient echoes. The sequence was timed such that all data acquisition occurred during end diastole, and the inversion delay was iteratively chosen to null the signal from normal myocardium. Other acquisition parameters were 7/3; flip angle, 15°; field of view, 340–400 mm; matrix, 256 x 256; section thickness, 8–10 mm; 16 images collected per heartbeat; two signals acquired; and total acquisition time, 16 heartbeats per section. The first temporal moment of the gradient waveforms along the section-select and the frequency-encoding directions were zero.

Data Analysis
Quantitative analysis.—The infarcted areas of irreversibly damaged myocardium were identified on the delayed-enhancement MR images as regions of increased signal intensity (at least two times higher than that of remote normal myocardium). An experienced radiologist (S.D.F.) with 10 years of experience in cardiovascular MR imaging drew regions of interest to circumscribe the area of infarction on delayed-enhancement MR images. Additional regions of interest (area, 15–20 square pixels) were drawn to include (a) normal remote myocardium identified on the delayed-enhancement images as regions without enhancement and (b) the midventricular blood pool (area, 20–40 square pixels).

The regions of interest were drawn to minimize the influence of signal intensity variations caused by surface coil reception fall-off away from the coil surface. These regions of interest were then copied to the end-diastolic phase of T1{rho}- and T1-weighted cine turbo field-echo sections acquired at identical orientations. Means and SDs within the region of interest were calculated for each tissue type and for each technique.

The following quantitative indexes were defined: (a) the ratio of the signal intensity of blood to that of normal myocardium and (b) percentage enhancement, defined as the ratio of signal intensity difference between infarcted and normal myocardium to the signal intensity of normal myocardium times 100. These indexes were calculated for all three techniques: delayed enhancement, T1{rho}-weighted turbo field echo, and T1-weighted turbo field echo.

Statistical Analysis
All values are reported as mean ± 1 SD. A two-tailed paired Student t test was used to test whether (a) the signal intensity ratio of blood to normal myocardium estimated from T1- and T1{rho}-weighted turbo field-echo sequences was statistically different and (b) percentage enhancement estimated from T1- and T1{rho}-weighted turbo field-echo images was statistically different. For all statistical tests, a P value less than .05 was considered to reflect statistical significance.


   Results
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
Discussion
 REFERENCES
 
In all patients (n = 21) imaged with T1{rho}-weighted turbo field-echo MR sequences, the signal intensity ratio of blood to normal myocardium was 3.2 ± 0.8, and the contrast between infarcted and normal myocardium, expressed as percentage enhancement, was 66% ± 39. In 12 patients in whom a direct comparison with conventional turbo field-echo cine MR imaging data without T1{rho} application was available, T1{rho}-weighted turbo field-echo MR images provided a signal intensity ratio of blood to normal myocardium of 3.5 ± 0.9, compared with 2.3 ± 0.7 with standard T1-weighted imaging (P < .004). With T1{rho} weighting, the percentage enhancement of the irreversibly injured myocardium was 68% ± 41, compared with 23% ± 24 without T1{rho} weighting (P < .006) (Fig 2).



View larger version (26K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2. Diagram indicates contrast between injured and normal myocardium by using the T1{rho}-weighted cine turbo field-echo (TFE) MR sequence, expressed as percentage enhancement. Note improved contrast between the two tissues with T1{rho}-weighted MR imaging compared with conventional MR imaging in all but one patient, who had microvascular obstruction.

 
In terms of percentage enhancement, the delayed-enhancement technique provided substantially higher contrast between normal and infarcted myocardium (percentage enhancement, 588% ± 344; n = 21) compared with that of the T1{rho}-weighted cine sequence. Qualitatively, the infarcted regions were conspicuous on the cine images and were concordant with infarction on delayed-enhancement images in both size and location. Some representative clinical results are shown in Figures 3 and 4.



View larger version (45K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3. Region of acute myocardial infarction (arrow) in a 32-year-old man with 3-day-old reperfused infarct. Infarction was identified in the region fed by the left circumflex artery (4 o’clock) as a zone of increased signal intensity at delayed-enhancement MR imaging (7/3; flip angle, 15°; inversion-recovery prepulse followed by a segmented k-space readout) in this short-axis image obtained at the midventricular level (left). The same region is well delineated on the T1{rho}-weighted cine turbo field-echo MR image (5.1/2.2; flip angle, 25°; composite radiofrequency pulse for T1{rho} weighting) (middle) compared with a conventional cine turbo field-echo MR image (right) (5/2; flip angle, 25°).

 


View larger version (68K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 4. Region of acute myocardial infarction (arrows) in a 45-year-old man with a 2-day-old reperfused infarct, which was identified in the territory covered by the left anterior descending artery as a patchy zone of increased signal intensity on the delayed-enhancement MR image (7/3; flip angle, 15°; inversion-recovery prepulse followed by a segmented k-space readout), which reflects damage to the apex, distal two-thirds of the anterior wall, and distal inferoseptal wall (left) in this two-chamber long-axis view. The same region is well delineated on the T1{rho}-weighted cine turbo field-echo MR image (5.1/2.2; flip angle, 25°; composite radiofrequency pulse for T1{rho} weighting) (middle) compared with a conventional cine turbo field-echo MR image (5/2; flip angle, 25°) (right).

 

   Discussion
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
REFERENCES
 
The precise mechanism by which T1{rho} weighting improves the contrast between irreversibly injured myocardium and normal myocardium on contrast-enhanced cine MR images is yet to be determined. Presumably, T1{rho} relaxation probes water spins in close interaction with macromolecules (13,14). Roughly 80% of the cell volume within an intact myocyte is composed of macromolecules—for example, structural and contractile proteins and mitochondria.

After infarction, myocardial cell death occurs by means of either necrosis caused by sarcolemmal membrane rupture or apoptosis manifesting as nuclear disintegration, cell shrinkage, and phagocytosis (19). The relative contributions of necrosis and apoptosis to myocardial cell death are uncertain. Nevertheless, in either case, the leakage of intracellular proteins caused by sarcolemmal rupture or nuclear cleavage alters the proton-macromolecular interaction. We speculate that this alteration minimizes the influence of macromolecules on proton relaxation and prolongs the T1{rho} of infarcted myocardium, making it a marker for acute myocardial infarction.

The results of our study show that contrast of blood to normal myocardium is improved with T1{rho} weighting as a result of greater suppression of normal myocardium. These results are consistent with findings of Dixon et al (21), who demonstrated improved contrast between normal myocardium and blood on contrast-enhanced cine MR images by using T1{rho} weighting. It has been shown previously in the context of neurologic imaging that magnetization transfer effect can be used synergistically for tissue-specific suppression in conjunction with gadolinium-based enhancement to delineate pathologic findings (22,23). We speculate that a similar synergistic mechanism may be at play with T1{rho} preparation. It has also been suggested that some of the T1{rho} effect is a manifestation of the underlying magnetization transfer effect between macromolecules and free water (14). In fact, magnetization transfer effect has been proposed as a means to identify infarcted myocardium (24). Recently, Weiss et al (25) demonstrated a method of using an off-resonance magnetization transfer contrast pulse and gadopentetate dimeglumine enhancement in a cine MR sequence to evaluate viability and function in a canine infarct model.

In delayed-enhancement MR imaging, the appearance of patchy, dark regions without contrast enhancement that are surrounded by fully enhanced regions has been reported to be consistent with regions of microvascular obstruction (26). In one patient with substantial microvascular obstruction, T1{rho}-weighted turbo field-echo MR imaging depicted these regions as areas with lower signal intensity and demonstrated a reduction in percentage enhancement (Fig 2). It has been suggested that the presence of microvascular obstruction is a good predictor of increased postinfarction cardiovascular complications (26).

A limitation of our study is the lack of a standard of reference other than delayed-enhancement imaging. The limitations of using T1{rho}-weighted turbo field-echo MR imaging for identification of acute myocardial infarction are as follows. First, similar to the findings of Simonetti et al (27), our results show that the contrast between infarcted and normal myocardium is high on delayed-enhancement MR images. While the infarcts were clearly visible on T1{rho}-weighted turbo field-echo cine MR images, the higher contrast of delayed-enhancement images, in principle, can extend the lower threshold of detection of small infarcts by using the delayed-enhancement technique.

Second, the spatial resolution of the delayed-enhancement technique, without the constraints of cine imaging, is much higher than that of the T1{rho}-weighted turbo field-echo sequence. This makes it possible to clearly delineate small, subendocardial infarcts that may be difficult to visualize by using the T1{rho}-weighted cine turbo field-echo sequence because of its lower spatial resolution, as well as the background of high blood signal intensity in the left ventricular cavity.

Our initial results show that T1{rho} weighting is a marker for characterization of myocardial infarction on the basis of a mechanism different from that used in delayed-enhancement MR imaging. Further efforts are necessary to optimize the T1{rho}-weighted MR sequence and to quantitate the differences in relaxation rate in the rotating frame (R1{rho} = 1/T1{rho}) between normal and irreversibly injured myocardium in the acute setting. In addition, the frequency dependence of T1{rho} (T1{rho} dispersion) may also serve as a tissue characterization parameter, as has been used in the identification of diseased muscle tissue (28) and more recently in the early detection of irreversible cerebral ischemia (18).

In conclusion, our results show that it is possible to add T1{rho} weighting to a conventional turbo field-echo cine MR sequence to improve the contrast between acutely infarcted and noninfarcted myocardium. Further studies are required to quantitatively determine the T1{rho}-weighted differences between normal and acutely infarcted myocardium.


   ACKNOWLEDGMENTS
 
The authors gratefully acknowledge the help of Brenda Lambert, RN, in recruiting patients and Vei Vei Lee, MS, from the Biostatistics Department for her technical assistance.


   FOOTNOTES
 
2 Current address: General Electric Corporate Research and Development, Schenectady, NY. Back

Author contributions: Guarantors of integrity of entire study, R.M., S.D.F.; study concepts and design, all authors; literature research, R.M., W.T.D.; clinical studies, S.D.F., J.M.W., R.I.P.; data acquisition, R.M., S.D.F.; data analysis/interpretation, all authors; statistical analysis, R.M., S.D.F.; manuscript preparation and definition of intellectual content, all authors; manuscript editing, R.M., S.D.F.; manuscript revision/review and final version approval, all authors


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 

  1. Higgins C, Herfkens R, Lipton M, et al. Nuclear magnetic resonance imaging of acute myocardial infarction in dogs: alterations in magnetic relaxation times. Am J Cardiol 1983; 52:184-188.[CrossRef][Medline]
  2. de Roos A, Dornbos J, van der Wall E, van Voorthuisen A. MR imaging of acute myocardial infarction: value of Gd-DTPA. AJR Am J Roentgenol 1988; 150:531-534.[Abstract/Free Full Text]
  3. de Roos A, van Rossum AC, van der Wall E, et al. Reperfused and nonreperfused myocardial infarction: diagnostic potential of Gd-DTPA enhanced MR imaging. Radiology 1989; 172:717-720.[Abstract/Free Full Text]
  4. van Rossum A, Visser F, van Eenige M, et al. Value of Gd-DTPA dynamics in magnetic resonance imaging of acute myocardial infarction with occluded and reperfused coronary arteries after thrombolysis. Am J Cardiol 1990; 65:845-851.[CrossRef][Medline]
  5. Lima J, Judd R, Bazille A, Schulman S, Atalar E, Zerhouni E. Regional heterogeneity of human myocardial infarcts demonstrated by contrast enhanced MRI: potential mechanisms. Circulation 1995; 92:1117-1125.[Abstract/Free Full Text]
  6. Kim RJ, Chen EL, Lima JA, Judd RM. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation 1996; 94:3318-3326.[Abstract/Free Full Text]
  7. Pereira R, Prato F, Wisenberg G, Sykes J. The determination of myocardial viability using Gd-DTPA in a canine model of acute myocardial ischemia and reperfusion. Magn Reson Med 1996; 36:684-693.[Medline]
  8. Rehwald WG, Fieno DS, Chen EL, Kim RJ, Judd RM. Myocardial magnetic resonance imaging contrast agent concentrations after reversible and irreversible ischemic injury. Circulation 2002; 105:224-229.[Abstract/Free Full Text]
  9. Kim RJ, Fieno DS, Chen EL, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999; 100:1992-2002.[Abstract/Free Full Text]
  10. Fieno DS, Kim RJ, Chen EL, et al. Contrast-enhanced magnetic resonance imaging of myocardium at risk: distinction between reversible and irreversible injury throughout infarct healing. J Am Coll Cardiol 2000; 36:1985-1991.[Abstract/Free Full Text]
  11. Hsu EW, Xue R, Holmes A, et al. Delayed reduction of tissue water diffusion after myocardial ischemia. Am J Physiol 1998; 275:H697-H702.
  12. Delepine S, Furber AP, Beygui F, et al. 3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI. Am J Physiol Heart Circ Physiol 2003; 284:H1190-H1197.[Abstract/Free Full Text]
  13. Sepponen RE, Pohjonen JA, Sipponen JT, Tanttu JI. A method for T1 rho imaging. J Comput Assist Tomogr 1985; 9:1007-1011.[Medline]
  14. Brown RD, 3rd, Koenig SH. 1/T1 rho and low-field 1/T1 of tissue water protons arise from magnetization transfer to macromolecular solid-state broadened lines. Magn Reson Med 1992; 28:145-152.[Medline]
  15. Duvvuri U, Charagundla SR, Kudchodkar SB, et al. Human knee: in vivo T1(rho)-weighted MR imaging at 1.5 T—preliminary experience. Radiology 2001; 220:822-826.[Abstract/Free Full Text]
  16. Halavaara JT, Lamminen AE, Bondestam S, et al. Spin lock magnetic resonance imaging in the differentiation of hemangiomas and metastases. Br J Radiol 1995; 68:1198-1203.[Abstract]
  17. Markkola AT, Aronen HJ, Paavonen T, et al. Spin lock and magnetization transfer imaging of head and neck tumors. Radiology 1996; 200:369-375.[Abstract/Free Full Text]
  18. Grohn OHJ, Kettunen MI, Makela HI, et al. Early detection of irreversible cerebral ischemia in the rat using dispersion of the magnetic resonance imaging relaxation time, T1rho. J Cereb Blood Flow Metab 2000; 20:1457-1466.[CrossRef][Medline]
  19. Opie LH. The heart physiology, from cell to circulation Philadelphia, Pa: Lippincott-Raven, 1998.
  20. Nomenclature and criteria for diagnosis of ischemic heart disease: report of the Joint International Society and Federation of Cardiology/World Health Organization task force on standardization of clinical nomenclature. Circulation 1979; 59:607-609.[Free Full Text]
  21. Dixon WT, Oshinski JN, Trudeau JD, Arnold BC, Pettigrew RI. Myocardial suppression in vivo by spin locking with composite pulses. Magn Reson Med 1996; 36:90-94.[Medline]
  22. Tanttu JI, Sepponen RE, Lipton MJ, Kuusela T. Synergistic enhancement of MRI with Gd-DTPA and magnetization transfer. J Comput Assist Tomogr 1992; 16:19-24.[Medline]
  23. Mathews VP, King JC, Elster AD, Hamilton CA. Cerebral infarction: effects of dose and magnetization transfer saturation at gadolinium-enhanced MR imaging. Radiology 1994; 190:547-552.[Abstract/Free Full Text]
  24. Scholz T, Hoyt R, DeLeonardis J, Ceckler T, Balaban R. Water-macromolecular proton magnetization transfer in infarcted myocardium: a method to enhance magnetic resonance image contrast. Magn Reson Med 1995; 33:178-184.[Medline]
  25. Weiss CR, Aletras AH, London JF, et al. Stunned, infarcted, and normal myocardium in dogs: simultaneous differentiation by using gadolinium-enhanced cine MR imaging with magnetization transfer contrast. Radiology 2003; 226:723-730.[Abstract/Free Full Text]
  26. Wu KC, Zerhouni EA, Judd RM, et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation 1998; 97:765-772.[Abstract/Free Full Text]
  27. Simonetti OP, Kim RJ, Fieno DS, et al. An improved MR imaging technique for visualization of myocardial infarction. Radiology 2001; 218:215-223.[Abstract/Free Full Text]
  28. Lamminen AE, Tanttu JI, Sepponen RE, Pihko H, Korhola OA. T1 rho dispersion imaging of diseased muscle tissue. Br J Radiol 1993; 66:783-787.[Abstract]



This article has been cited by other articles:


Home page
 RadiologyHome page
D. C. Peters, J. V. Wylie, T. H. Hauser, K. V. Kissinger, R. M. Botnar, V. Essebag, M. E. Josephson, and W. J. Manning
Detection of Pulmonary Vein and Left Atrial Scar after Catheter Ablation with Three-dimensional Navigator-gated Delayed Enhancement MR Imaging: Initial Experience
Radiology, March 1, 2007; 243(3): 690 - 695.
[Abstract] [Full Text] [PDF]

Home page
 RadiologyHome page
G. L. Raff, W. W. O'Neill, R. E. Gentry, A. Dulli, K. G. Bis, A. N. Shetty, and J. A. Goldstein
Microvascular Obstruction and Myocardial Function after Acute Myocardial Infarction: Assessment by Using Contrast-enhanced Cine MR Imaging.
Radiology, August 1, 2006; 240(2): 529 - 536.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2322030334v1
232/2/606    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Muthupillai, R.
Right arrow Articles by Dixon, W. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muthupillai, R.
Right arrow Articles by Dixon, W. T.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
RADIOLOGY RADIOGRAPHICS RSNA JOURNALS ONLINE